Abstract
The relationship between vessel tone and cAMP production induced by vasoactive intestinal polypeptide (VIP), peptide histidine methionine (PHM), peptide histidine valine (PHV), pituitary adenylate cyclase activating polypeptide (PACAP-27 and PACAP-38), and neuropeptide Y (NPY) was investigated in rabbit ovarian arteries in vitro. VIP, PHM, PHV, PACAP-27, and PACAP-38 added in single-dose experiments (10 −9 , 10 −8 , 10 −7 , and 10 −6 M ) induced all a significant dose-related relaxation of noradrenaline (NA)-precontracted vessels and displayed similar potencies. VIP, PHM, PHV, PACAP-27, and PACAP-38 all increased cyclic adenosine monophosphate (cAMP) accumulation. The cAMP accumulation induced by PACAP-27 and PACAP-38 was five times higher than the cAMP content induced by the other three peptides. The peptide-induced smooth muscle relaxation did not correlate to the cAMP accumulation. NPY (10 −7 M ) markedly reversed the relaxations induced by VIP, PHM, PHV, PACAP-27, and PACAP-38, but did not influence the cAMP production induced by these peptides. In conclusion, the relaxation induced by VIP, PHM, PHV, PACAP-27, and PACAP-38 and the contraction induced by NPY are not solely related to the changes of cAMP contents. These findings indicate that in addition to cAMP, another intracellular signal transduction pathway may be involved in the relaxation and contraction induced by these peptides in rabbit ovarian artery.
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